Exciting research results have been obtained relating to peripheral nerve microenvironment, the blood nerve barrier and metabolic events which relate to the mechanism of fiber pathology in experimental and human diabetic polyneuropathy. Decreased blood flow and oxygen tension have been found in experimental diabetes by Dr. Low and colleagues. Decreased nerve conduction and resistance to ischemic nerve block can be partially prevented by oxygen supplementation. Similar alteration of nerve conduction and resistance to ischemic block can be achieved in normal rats by hypoxia alone. Dr. Low has produced convincing evidence that hypoxia might play an important role in functional alteration in diabetic polyneuropathy. Dyck and coworkers in human studies have shown that capillary closure and endothelial cell hypertrophy and proliferation are significantly more common in sural nerves of diabetic patients with neuropathy than in nerves of diabetics without neuropathy and than in healthy subjects. The two capillary abnormalities are significantly associated with quantitative neuropathologic measurements. These studies suggest that capillary abnormality is associated with fiber abnormality in human diabetic polyneuropathy. Morphometric studies appear to be showing that fiber loss is multifocal and distributed over the proximal to distal extent of nerves consistent with ischemic damage. Studies by Dr. Poduslo and coworkers are showing that endoneurial fluid albumin is increased in diabetic polyneuropathy, perhaps providing further evidence of altered capillaries in human diabetic neuropathy. Metabolic events involving lipids are explored by Dr. Holman, Dr. Schmid and Dr. Baumann and their colleagues.